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82 Cards in this Set
- Front
- Back
Salivary glands functions (3)
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Moistening
Buffer (ductal cells secrete bicarbonate) Amylase to break starch bonds |
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Enteric nervous system (myenteric vs submucosal plexi)
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Myenteric - between longitudinal and circular muscle layers, control over GI motility
Submucosal - senses lumen environment, regulates blood flow and epithelial cell functions |
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Gastrin (source, target, action)
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Source: Antrum of stomach
Target: Parietal cell in stomach Action: H+ and pepsinogen secretion |
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Cholecystokinin (CCK) (source, target, action)
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Source: Duodenum and jejunum
Target: Pancreas + gallbladder Action: Enzyme secretion, contraction |
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Secretin (source, target, action)
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Source: Duodenum
Target: Pancreatic and biliary ducts Action: Bicarb and fluid secretion |
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Gastrin-releasing peptide (source, target, action)
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Source: Vagal nerve endings
Target: Antrum of stomach Action: Gastrin release |
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Somatostatin (source, target, action)
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Source: Stomach + duodenum
Target: Stomach, liver, pancreas Action: Gastrin release, endocrine/exocrine secretions, bile flow |
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Gastric inhibitory pepitde
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Source: Duodenum and jejunum
Target: Pancreas Action: Decrease fluid absorption |
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Stomach secretions (5)
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H+ -cleaves pepsinogen
Pepsinogens Mucus Intrinsic factor (for B12) Water |
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Gastric pits
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Neck cells rich in mucus secretion
Basal cells: parietal secrete H+, chief (more basal) secrete pepsinogen |
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How is trypsinogen activated?
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Cleaved by enterokinase on enterocyte membranes
Cleaved trypsin is autocatalytic and can also cleave other pro-enzymes/zymogens |
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What causes contraction of the gallbladder during eating?
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CCK
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Bile acids (3)
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Primary and secondary (eg cholic and deoxycholic)
Amphipathic Interact w/ cholesterols and phospholipids to form micelles |
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Regulation of bile secretion (3)
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Vagus nerve stimulates liver bile production
Fatty acids and a.a. in chyme stimulate CCK secretion into blood -> gallbladder contraction Acidic chyme stimulates secretin into blood -> enhances flow of bicarb rich bile from liver |
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Epithelial cells in lining of small intestine (5)
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Absorptive - a.a., glucose, enzymes
Goblet - mucin Enterocyte - gastrin, cck, secretin Stem - cell renewal Paneth - lysozyme |
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Sugar absorption
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Na-coupled transport
Glucose/galactose/fructose |
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Protein absorption
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As small peptides and amino acids by membrane bound peptidases and specific transporters
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Fat absorption
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Cells take up hydrophobic materials from micelles
Pancreatic lipase -> MAGs -> glycerol and free FAs |
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Water absorption
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9 L pumped into GI tract per day
8 reabsorbed by small intestine 100 mL excreted in feces |
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Acromegaly and 2 facts about GH
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Excess growth hormone AFTER closure of epiphyseal plates
Gigantism results if excess is before Mediated by IGF-1 GH stimulates lipolysis in adipocytes |
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What type of hormone are the thyroid hormones?
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Amino acid derivatives
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Hormone half-lives and degradation
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Steroid - long, 1hr, degraded/conjugated in liver
Polypeptides - minutes, RME + lysosomal degradation Amino acid derivatives - Epi and Norepi in seconds, T3 in days |
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Types of cell-surface receptors
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Ion channel-linked (electrically excitable cells)
G protein-linked Enzyme-linked (mostly protein kinases) |
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G protein linked cell-surface receptors (3)
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Single polypeptide chain that spans membrane 7 times
Signal is relayed by heterotrimeric GTP binding proteins (G proteins) which are GTPases Regulate intracellular second messengers (cyclic AMP/GMP, Ca++) |
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Mechanisms of G protein receptors (4 steps)
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Inactive: G protein's α unit is bound to GDP
Ligand binds receptor and GDP is exchanged for GTP α unit detaches from G protein to interact w/ downstream targets Life time is short and GTP is quickly hydrolyzed to GDP with reassociation of alpha unit |
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cyclic AMP (effect, synth)
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Activates regulatory subunits of kinases
Synth'd by membrane-bound adenylate cyclase and rapidly destroyed by cAMP phosphodiesterase to 5'-AMP cAMP activates protein kinase A -> CREB |
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Calcium ion regulation (2 major pathways)
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Cells actively pump out
ER also has a pump to increase Ca concentration in ER 1. Nerve cell depolarization causes influx of Ca 2. Release of Ca from ER via IP3 |
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PIP2 (2 major effects)
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G-protein linked receptor initiates phospholipase C hydrolysis of PIP2
-> diacylglycerol (DAG) -> activates protein kinase C and -> IP3 -> release of Ca from ER |
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Enzyme-linked receptors (what 3 hormones?)
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Usually tyrosine kinases activated upon ligand-binding
Activated by dimerization or conformational change GH, Insuline, Epo all signal thru tyrosine kinases |
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What three hormones act through intracellular receptors?
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Steroids
Vitamin D Thyroid hormones |
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What does cGMP regulate? (2)
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Phototransduction
Smooth muscle contraction in response to NO |
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4 main kidney functions
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Filter blood to generate fluid free of cells and proteins
Reabsorb solutes and water from tubular fluid Secrete other solutes into tubular fluid Excrete via urine remaining water and solutes |
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Macula densa
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In distal tubule
Senses fluid flow Signals juxtaglomerular cells in afferent arteriole to produce renin |
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Juxtaglomerular cells
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Produce renin
Help control constriction of afferent and efferent arterioles |
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How does kidney control body fluid volume vs osmolality?
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Body fluid volume by Na excretion
Osmolality by water excretion |
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Excretion = ?
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Filtration - Reabsorption + Secretion
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Glomerular filtration rate
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20% of plasma is filtered into Bowman's space
125 mL/min |
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Renal plasma flow and filtration fraction
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Renal plasma flow = 650 mL/min
Filtration fraction = 20% = GFR/RPF |
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Renal clearance
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Volume of plasma per unit time from which X has been completely removed and exreted
Cx = Ux * V / Px U = concentration of x in urine V = urine flow rate Px = concentration of x in plasma |
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Excretion rate
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Ux * V
(so clearance = excretion rate / plasma concentration) |
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Measuring GFR
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Using inulin which is freely filtered and not absorbed or secreted
All of inulin is the result of filtration so rate of excretion = rate of filtration |
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Kidney regulation by norepinephrine (action, released in response to?)
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Vasoconstrictor of afferent and efferent arteriole
Released in response to decreased blood pressure or volume Decreases GFR and RBF |
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Kidney regulation by nitric oxide (action, released in response to?)
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Dilates afferent and efferent arterioles, increasing GFR and RBF
Released by endothelial cells in response to increased intake of NaCl |
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What is the primary driving force for Na uptake in the nephron?
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Na-K ATPase in basolateral membrane of epithelial cells keeps cytoplasmic Na concentration low
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Proximal tubule (3 and diabetes mellitus)
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Water and Na reabsorption
Isoosmotic: water follows Na passively Na transport is couple apically to H+ antiport and glucose symport If Pglucose > 2-3 mg/mL then cotransporters are overhwlemed and glucose appears in urine |
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Thin descending limb
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Highly permeable to water and interstitial fluid has high osmolarity
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Thin ascending limb
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Impermeable to water but permeable to Na and Cl passively
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Thick ascending limb (2)
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Na/K/2Cl transporter couples uphill movement of K and Cl to downhill movement of Na -- all 3 ions are reabsorbed
Paracellular cation absorption |
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Early distal tubule (2)
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Impermeable to water
Na/Cl symporter |
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Late distal tubule and collecting duct (3)
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Principle cells reabsorb Na and secrete K
High plasma osmolarity -> ADH secretion -> increased # water absorption channels and vice versa for low osmolarity |
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Diabetes insipidus
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No ADH response so consume lots of water to balance high excretion
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What happens if Na intake > Na excretion?
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Increased plasma osmolarity
Water form ICF to ECF Volume expansion --Volume contraction if intake < excretion |
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Sympathetic nerve activity (SNA)
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Stimulated by volume contraction
Increases renin secretion and Na reabsorption Decreases GFR |
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Renin/Angiotensin
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Stimulated by decreased afferent arteriole pressure
Renin cleaves angiotensinogen to angiontensin which is cleaved to angiotensin II by ACE Increases blood pressure and Na reabsorption |
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Aldosterone
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Stimulated by increased angiotensin I + Kplasma
Increases collecting duct Na reabsorption |
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ADH
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Stimulated by increased plasma osmolarity and volume contraction
Increases CD water reabsoprtion |
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Atrial natriuretic peptide (3)
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Stimulated by volume expansion
Increases GFR Decreases renin, aldo, ADH |
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Response decreased ECV (volume contraction)
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Up: SNA, renin, aldosterone, ADH
Down: ANP, Na/H2O excretion |
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K+ homeostasis
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Small rise in plasma K+
-> aldosterone -> increases K+ secretion by increasing Na-K ATPase in apical K+ channels in principal cells |
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Ca++ homeostasis
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Only regulated in late distal tube and CD, but taken up in all of nephron
Hypocalcemia -> calcitrol + PTH stimulate Ca absorption in gut and reabsorption in kidney |
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pH homeostasis in kidney
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Alpha intercalated cells of late distal tubule and CD contain ATP-driven proton pump to excrete H+
Also have Cl/HCO3 exchanger to secrete bicarb to interstitial fluid |
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Leydig cells (stimulated by, secrete, induce)
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Stimulated by chorionic gonadotrophin
Secrete testosterone (induces Wolffian duct) + DHT (Induces penis, prostate, urethra) |
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Sertoli cells
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Secrete mullerian inhibiting factor causing regression of mullerian duct
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Turner's and Klinefelter's
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Turner's - XO, , female phenotype w/ no ovaries/menses/puberty
Klinefelter's - XXY, male but sterile genitalia |
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Androgen resistance developmental disorder (3)
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Male
But can have complete development have normal female genitalia MIS was produced so lack Muellerian duct |
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Male puberty tanner stages
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I - prepuberty, pre adolescent
II - testicular enlargement, early pubic hair III - penile enlargement IV - growth of glans of penis V - complete adult genitalia |
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HPA axis basics
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Hypothalamus - GnRH
-> Pituitary - LH and FSH LH -> Leydig cells -> androgens FSH -> Sertoli cells -> spermatogenesis + inhibin feedbacks to ant. pit. |
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Androgen potency (4)
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DHT > testosterone > androstenedione > DHEA
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Stages in female puberty
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Thelarche - breast development
Pubarche - development of pubic hair Menarche - onset of menstruation |
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HPA axis in females
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LH -> theca cells -> androgens/progestins
FSH -> granulosa cells -> estrogens, progestins, inhibins/activins |
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4 functions of placenta
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Hormones: hCG, hCS
Gas transport Solute transport Storage functions |
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Mother’s contribution to materno-placental-fetal unit
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Provides LDL as precursor for steroid hormones
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Placental contribution to materno-placental-fetal unit (2)
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Produces estrogen and progesterone from maternal LDL
Produces pregnenalone for fetal steroid synthesis |
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Fetal contribution to materno-placental-fetal unit
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Synth DHEAS which is transferred back to placenta for estrogen synth
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Parturition: prostaglandins (3)
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Stimulate uterine contractions
Softening/dilation/thinning of cervix Used to induce labor |
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Parturition: oxytocin (3)
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Augments labor
Ferguson reflex - distension of cervix Constricts uterine blood vessels where placenta used to be |
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Parturition: positive feedback loop (5)
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Cervical stretch -> Oxytocin -> Prostaglandins from uterine wall -> uterine contractions -> cervical stretch
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Breast changes during pregnancy
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Rising estrogen, progesterone, prolactin increase breast water, electrolyte and protein
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Lactation: estrogen
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Ductal proliferation facilitated by prolactin
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Lactation: progesterone
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Acinar epithelial differentiation
Facilitated by estrogen |
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3 hormones necessary for milk production after lactation
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Prolactin, oxytocin, cortisol
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Neural pathways of lactation stimulation (Oxytocin and prolactin)
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Suckling -> afferent to mesencephalon -> releases dopamine inhibition -> allows prolactin synthesis
afferents also directly stimulate oxytocin release |